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      The Coronary Effects of Parathyroid Hormone

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          Objective: The aim of the present study was to characterize the role of the ATP-sensitive potassium channels (K<sup>+</sup><sub>ATP</sub>) in the coronary dilator action of parathyroid hormone (PTH). Methods: Dose-response curves of intracoronary administrated PTH (0.15–1.33 nmol) were obtained in control phases and during continuous intracoronary administration of the K<sup>+</sup><sub>ATP</sub> channel-selective antagonist glibenclamide (0.1–1.0 µmol/min) in dogs (n = 13). Results: Increments of integrated coronary conductance (excess coronary conductance) at PTH doses of 0.15 and 1.33 nmol were 1.17 versus 0.03 ml/mm Hg (p < 0.05) and 4.03 versus 0.94 ml/mm Hg (p < 0.05) in the control versus during maximal blockade, respectively. Conclusion: The results indicate that the activation of K<sup>+</sup><sub>ATP</sub> channels significantly contributes to the PTH-induced coronary vasodilation.

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          Arterial dilations in response to calcitonin gene-related peptide involve activation of K+ channels.

          Calcitonin gene-related peptide (CGRP) is a 37-amino-acid peptide produced by alternative processing of messenger RNA from the calcitonin gene. CGRP is one of the most potent vasodilators known. It occurs in and is released from perivascular nerves and has been detected in the blood stream, suggesting that it is important in the control of blood flow. The mechanism by which it dilates arteries is not known. Here, we report that arterial dilations in response to CGRP are partially reversed by blockers of the ATP-sensitive potassium channel (K(ATP)), glibenclamide and barium. We also show that CGRP hyperpolarizes arterial smooth muscle and that blockers of K(ATP) channels reverse this hyperpolarization. Finally, we show that CGRP opens single K+ channels in patches on single smooth muscle cells from the same arteries. We propose that activation of K(ATP) channels underlies a substantial part of the relaxation produced by CGRP.
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            PKA-mediated phosphorylation of the human K(ATP) channel: separate roles of Kir6.2 and SUR1 subunit phosphorylation.

            ATP-sensitive potassium (K(ATP)) channels play important roles in many cellular functions such as hormone secretion and excitability of muscles and neurons. Classical ATP-sensitive potassium (K(ATP)) channels are heteromultimeric membrane proteins comprising the pore-forming Kir6.2 subunits and the sulfonylurea receptor subunits (SUR1 or SUR2). The molecular mechanism by which hormones and neurotransmitters modulate K(ATP) channels via protein kinase A (PKA) is poorly understood. We mutated the PKA consensus sequences of the human SUR1 and Kir6.2 subunits and tested their phosphorylation capacities in Xenopus oocyte homogenates and in intact cells. We identified the sites responsible for PKA phosphorylation in the C-terminus of Kir6.2 (S372) and SUR1 (S1571). Kir6.2 can be phosphorylated at its PKA phosphorylation site in intact cells after G-protein (Gs)-coupled receptor or direct PKA stimulation. While the phosphorylation of Kir6.2 increases channel activity, the phosphorylation of SUR1 contributes to the basal channel properties by decreasing burst duration, interburst interval and open probability, and also increasing the number of functional channels at the cell surface. Moreover, the effect of PKA could be mimicked by introducing negative charges in the PKA phosphorylation sites. These data demonstrate direct phosphorylation by PKA of the K(ATP) channel, and may explain the mechanism by which Gs-coupled receptors stimulate channel activity. Importantly, they also describe a model of heteromultimeric ion channels in which there are functionally distinct roles of the phosphorylation of the different subunits.
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              Clinical experience with percutaneous ethanol injection therapy in hemodialysis patients with renal hyperparathyroidism.

              Percutaneous ethanol injection therapy (PEIT) is a noteworthy method to treat patients with renal hyperparathyroidism (RHPT). This study was performed to enable the authors to propose appropriate indications for PEIT.

                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                April 2004
                23 April 2004
                : 61
                : 5
                : 234-241
                Experimental Research Laboratory, Department of Cardiovascular Surgery, Semmelweis University Budapest, Budapest, Hungary
                76628 Horm Res 2004;61:234–241
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 5, References: 40, Pages: 8
                Original Paper


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